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Genetic Basis of Streptococcin A-FF22 Production

By J. R. Tagg and L. W. Wannamaker

Abstract

Spontaneous, low-frequency loss of ability to produce streptococcin A-FF22 (SA) by group A streptococcus strain FF22 was observed. The proportion of non-SA-producing (SA(−)) derivatives occurring in strain FF22 cultures grown in Todd Hewitt broth supplemented with 1% of yeast extract (THBY) was increased on treatment with ethidium bromide, acriflavin, or rifampin. The highest incidence of SA(−) organisms, however, was found in untreated THBY cultures that had been aging by incubation at 37°C for several months. The possibility of selective effects in these experiments, operating to enhance the apparent frequency of SA(−) bacteria, was discounted. The survival of SA(−) derivatives in association with populations of SA(+) bacteria was dependent upon the use of culture conditions inimical to SA activity, since a consistent finding was that the loss of ability to produce SA was associated with loss of immunity to the killing action of this bacteriocin. Whereas selective killing of SA(−) derivatives was evident in mixed cultures of SA(+) and SA(−) strains in tryptic soy broth, no such effect was demonstrable in THBY. In these experiments, elimination of SA(−) cells seemed directly related to the presence of active SA. Purified clones of SA(−) substrains did not seem revertible to SA production, either spontaneously or on treatment with nitrosoguanidine. It is suggested that the property of production of SA by group A streptococcus strain FF22, together with that of host cell immunity to the homologous bacteriocin, may be mediated by plasmid-borne genetic determinants

Topics: Biosynthesis; Chemistry; Mechanisms of Action and Resistance
Year: 1976
DOI identifier: 10.1128/aac.10.2.299
OAI identifier: oai:pubmedcentral.nih.gov:429739
Provided by: PubMed Central
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